Adrenergic receptors in insensitive skin of spinal cord injured patients.

The factors responsible for the increased susceptibility to decubitus ulcers of the insensitive skin of spinal cord injury (SCI) patients are not known. Autonomic dysfunction leading to defective vascularity is a possibility. SCI removes cerebral control of the isolated nervous system which may mimic denervation hypersensitivity of autonomic neural synapses, where an increase in number and a scattering of the receptors on the postsynaptic membrane leads to abnormal responses. Since adrenergic receptors mediate vascular tone and regulate blood flow in the skin, it would be of great interest to determine whether the number and the concentration of receptors in the insensitive skin of SCI patients is modified as a function of time since injury. To achieve this aim, alpha and beta adrenergic receptors were measured in biopsies obtained from intact skin used to surgically repair decubitus ulcers in SCI patients admitted to The Institute for Rehabilitation and Research. Receptors were identified by competitive radioligand-binding assays in whole skin homogenates. Patients were divided into two groups: patients injured less than five years ("early") and patients injured more than five years ("late"). Alpha and beta adrenergic receptors in both cervical and thoracic SCI patients decreased in density in the "late" patients. The small sample size and the inherent large errors of the assay precluded achievement of statistically significant differences. Nevertheless, a definite trend is seen: Disconnection of the adrenergic neurons from brain integration may mimic denervation and lead to abnormal vascular responses in the insensitive skin.